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PRC2 recruitment and H3K27me3 deposition at FLC require COOLAIR Binding by FCA

Yongke Tian  Han Zheng  Fei Zhang  Shiliang Wang  Xiaoru Ji  Yuehui He  Yong Ding  
【摘要】:The cold-induced antisense transcript COOLAIR represses FLOWERING LOCUS C(FLC) transcription by modulating histone H3 methylation,causing increasedH3 K27 me3 and decreased H3 K36 me3 levels in response to cold temperatures.However,the molecular connection between COOLAIR and histone modification factors in the absence of cold treatment remains unclear.Here,we report that the RNAbinding protein FLOWERING CONTROL LOCUS A(FCA) interacts with the Polycomb Repressive Complex 2(PRC2) subunit CURLY LEAF(CLF) and binds nascent COOLAIR transcripts to allow deposition of H3 K27 me3 at FLC.Loss of FCA function leads to a reduction in CLF enrichment and H3 K27 me3 deposition at FLC.FCA directly binds to COOLAIR and loss of COOLAIR function results in a reduction in FCA and CLF enrichment,which in turn decreases H3 K27 me3 levels at FLC.The Arabidopsis protein phosphatase SSU72 physically interacts with the RRM1 motif of FCA to antagonize FCA binding with COOLAIR.Mutations in SSU72 result in early flowering,reduced FLC transcription,increased CLF enrichment and H3 K27 me3,and enhanced affinity between FCA and COOLAIR.Our results provide new insight into how FCA and SSU72 coordinately regulate H3 K27 me3 via COOLAIR and suggest that the binding between COOLAIR and FCA is critical for PRC2 enrichment andH3 K27 me3 deposition in Arabidopsis.

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